TY - JOUR
T1 - Maresin 1 Resolves Inflammation and Aids Bone Healing in Periapical Lesions
AU - Demir, E.
AU - İlgenli, I.
AU - Guney, Z.
AU - Mohammadi, S.
AU - Lauwens, K.
AU - Yakar, N.
AU - Alvarez Rivas, C.
AU - Unlu, O.
AU - Kantarci, A.
N1 - Publisher Copyright:
© The Author(s) 2025. This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).
PY - 2026/8
Y1 - 2026/8
N2 - Chronic apical periodontitis (CAP) is a persistent inflammatory condition caused by microbial infections in the root canal system, leading to bone loss and tissue damage. In this study, we tested the hypothesis that maresin 1 (MaR1), a specialized proresolving mediator, facilitates inflammatory resolution and promotes bone healing in CAP. We developed a CAP model in mice through pulp exposure. Animals received intracanal administration of either MaR1 or a vehicle. Micro–computed tomography (micro-CT) was used to analyze lesion size and bone volume changes. Inflammatory cell infiltration was assessed in hematoxylin and eosin–stained sections, and microbial diversity was analyzed using next-generation sequencing. The role of regulatory T cells (Tregs) was further explored through diphtheria toxin–induced depletion of Tregs in Foxp3eGFP/IL17 transgenic mice. All statistical analyses were performed using parametric methods, as confirmed by the Shapiro–Wilk test for data normality. Analysis of variance with Tukey’s post hoc and Bonferroni-corrected t tests was applied. P < 0.05 was considered significant. In 2-dimensional analyses, a significant difference was observed between the control and lesion groups, supporting the validity of the experimental model. MaR1 treatment significantly reduced lesion size (P < 0.0001). The bone volume/total volume ratio was significantly higher in the MaR1 group than in the vehicle group (P < 0.05). Bone mass was reduced in the lesion group, whereas MaR1 treatment significantly alleviated this loss (P < 0.05). The number of inflammatory cells was significantly lower in the MaR1 group compared to the vehicle group (P < 0.05). MaR1 also reduced Enterococcus faecalis, a key pathogen in persistent infections. This study highlights MaR1 as a promising treatment for chronic apical periodontitis, showing benefits in resolving inflammation, preserving bone, and reducing E. faecalis. Unlike conventional therapies, MaR1 supports immune modulation and tissue repair.
AB - Chronic apical periodontitis (CAP) is a persistent inflammatory condition caused by microbial infections in the root canal system, leading to bone loss and tissue damage. In this study, we tested the hypothesis that maresin 1 (MaR1), a specialized proresolving mediator, facilitates inflammatory resolution and promotes bone healing in CAP. We developed a CAP model in mice through pulp exposure. Animals received intracanal administration of either MaR1 or a vehicle. Micro–computed tomography (micro-CT) was used to analyze lesion size and bone volume changes. Inflammatory cell infiltration was assessed in hematoxylin and eosin–stained sections, and microbial diversity was analyzed using next-generation sequencing. The role of regulatory T cells (Tregs) was further explored through diphtheria toxin–induced depletion of Tregs in Foxp3eGFP/IL17 transgenic mice. All statistical analyses were performed using parametric methods, as confirmed by the Shapiro–Wilk test for data normality. Analysis of variance with Tukey’s post hoc and Bonferroni-corrected t tests was applied. P < 0.05 was considered significant. In 2-dimensional analyses, a significant difference was observed between the control and lesion groups, supporting the validity of the experimental model. MaR1 treatment significantly reduced lesion size (P < 0.0001). The bone volume/total volume ratio was significantly higher in the MaR1 group than in the vehicle group (P < 0.05). Bone mass was reduced in the lesion group, whereas MaR1 treatment significantly alleviated this loss (P < 0.05). The number of inflammatory cells was significantly lower in the MaR1 group compared to the vehicle group (P < 0.05). MaR1 also reduced Enterococcus faecalis, a key pathogen in persistent infections. This study highlights MaR1 as a promising treatment for chronic apical periodontitis, showing benefits in resolving inflammation, preserving bone, and reducing E. faecalis. Unlike conventional therapies, MaR1 supports immune modulation and tissue repair.
KW - bone regeneration
KW - immune modulation
KW - microbial diversity
KW - periapical periodontitis
KW - resolution of inflammation
KW - specialized proresolving mediators
UR - https://www.scopus.com/pages/publications/105025001009
U2 - 10.1177/00220345251399558
DO - 10.1177/00220345251399558
M3 - Article
C2 - 41408494
AN - SCOPUS:105025001009
SN - 0022-0345
VL - 105
SP - 1163
EP - 1173
JO - Journal of Dental Research
JF - Journal of Dental Research
IS - 9
ER -